alexa Targeting the PD-1 Pathway in MSI-Stable Metastatic Col
ISSN: 2167-7700

Chemotherapy: Open Access
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Editorial

Targeting the PD-1 Pathway in MSI-Stable Metastatic Colorectal Cancer

Kaijun Huang1 and Jennifer Wu2*

1Department of Medicine, NYU Lutheran Medical Center, Brooklyn, NY, USA

2Department of Medicine, Division of Hematology-Oncology, Laura and Isaac Perlmutter Cancer Center, New York, NY, USA

*Corresponding Author:
Jennifer Wu
Department of Medicine, Division of Hematology-Oncology, Laura and Isaac Perlmutter Cancer Center
NYU School of Medicine 462 First Avenue, New York, NY 10016
Tel: 212-263-6485
E-mail: [email protected]

Received date: January 05, 2017; Accepted date: February 10, 2017; Published date: February 17, 2017

Citation: Huang K and Wu J (2017) Targeting the PD-1 Pathway in MSI-Stable Metastatic Colorectal Cancer. Chemo Open Access 6:e132. doi: 10.4172/2167-7700.1000e132

Copyright: © 2017 Huang K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

In patients with microsatellite instability-high (MSI-H) metastatic colorectal cancer (CRC), the inhibition of programmed death-1 (PD-1) pathway has achieved promising response [1]. PD-1 is an immune inhibitory receptor, expressed in many cells, including T cells. Its ligand, PD-L1, is expressed on surface of several cell types, especially tumor cells. When PD-L1 binds to PD-1, an inhibitory signal is transmitted into the T cell, which suppresses T-cell proliferation. MSIH metastatic CRC gives rise to high percentage of mutations which is proportional to mutational load. High mutational load of MSI-H CRC correlates with increased PD-L1 expression which indicates a higher likelihood of response to PD-1 inhibitors, compared to microsatellite instability-stable (MSI-S) CRC [2-4]. Нus, MSI-H CRC could respond to single agent PD-1 pathway inhibition.

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